Titlebook: Chromosomal Alterations; Methods, Results and Günter Obe,Vijayalaxmi Book 2007 Springer-Verlag Berlin Heidelberg 2007 Aberrationen, chromos

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https://doi.org/10.1007/978-3-642-88062-9ng it (“indirect effect,” mainly owing to the formation of ?OH radicals). These ionization events induce a series of free-radical reactions that eventually show up in biological end points such as mutations and reproductive cell death. Precursors of these biological end points are various kinds of d

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https://doi.org/10.1007/978-3-642-88062-9 and repair events or as potentially lethal lesions introduced by ionising radiation or drugs. In any case, DSBs have to be eliminated immediately, because of the recombinogenic capacity of the DNA ends generated by the DSB that increases the risk for undesired chromosomal aberrations (CAs). In orde

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Red Cell Structure and Its Breakdown,energy in the nucleus of the irradiated cell causing DNA double-strand cleavage and the failure of the DNA repair machinery to faithfully restore the integrity of the genetic material. There is also increasing evidence that an irradiated cell can signal to a non-irradiated “bystander” cell and elici

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Protoplasmatologia‘ Cell Biology Monographseing used in cancer therapy. Methylating agents attack DNA at 13 sites. The main mutagenic and carcinogenic DNA lesion is .-methylguanine, whereas both N-methylation lesions and .-methylguanine contribute to sister-chromatid exchanges, chromosomal aberrations and cell death. The contribution depends

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Triggers for the Transfusion of Red Cells,ion of sister-chromatid exchanges (SCE) and mutations following benzo[.]pyrene (BaP) exposure. Mean adduct levels per dose unit after exposure in vitro were higher in both human (11 studies) and animal (five studies) cells for doses below 5?μM (2.47 and 1.445 adducts per 10. nucleotides per μM, resp